Heat shock protein 90 inhibition results in altered downstream signaling of mutant KIT and exerts synergistic effects on Kasumi-1 cells when combining with histone deacetylase inhibitor

被引：19
|
作者：
Yu, Wenjuan [1 ]
Wang, Jianxiang [2 ,3 ,4 ]
Jin, Jie [1 ]
Qian, Wenbin [1 ]
Qian, Jiejing [1 ]
Cheng, Yizhi [1 ]
Wang, Lei [1 ]
机构：
[1] Zhejiang Univ, Sch Med, Dept Hematol, Affiliated Hosp 1, Hangzhou 310003, Zhejiang, Peoples R China
[2] Chinese Acad Med Sci, Inst Hematol, State Key Lab Expt Hematol, Tianjin, Peoples R China
[3] Chinese Acad Med Sci, Blood Dis Hosp, Tianjin, Peoples R China
[4] Peking Union Med Coll, Tianjin, Peoples R China
来源：
LEUKEMIA RESEARCH | 2011年 / 35卷 / 09期
基金：
高等学校博士学科点专项科研基金;
关键词：
Acute myeloid leukemia; KIT; Heat shock protein 90; Histone deacetylase inhibitor17-Allylamino-17-demethoxygeldanamycin; Two-hit; ACUTE MYELOID-LEUKEMIA; PHASE-I TRIAL; ADVANCED CANCER; 17-ALLYLAMINO-17-DEMETHOXYGELDANAMYCIN; HSP90; GELDANAMYCIN; STI-571; COMPLEX; DIFFERENTIATION; ASSOCIATION;
D O I：
10.1016/j.leukres.2011.05.014
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
KIT mutations may be associated with a poor prognosis in t(8;21) AML. Heat shock protein 90 (Hsp90) is a molecular chaperone frequently used by cancer cells to stabilize mutant oncoproteins. Inhibition of Hsp90 by 17-allylamino-17-demethoxygeldanamycin (17-AAG) disrupted downstream signaling pathways of mutant KIT in Kasumi-1 cells. AML1-ETO fusion gene and mutated KIT act as "two-hit" factors in Kasumi-1 cells. Histone deacetylation (HDAC) inhibitors sodium phenylbutyrate (PB) and valproic acid (VPA) block AML1-ETO. Co-treatment with 17-AAG and PB or 17-AAG and VPA resulted in a synergistic effect in Kasumi-1 cells. Our results confirmed that Hsp90 and mutated KIT were valid molecular targets in the therapy of AML. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码：1212 / 1218
页数：7
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